ap 5

AP-C5 is a compound with selective inhibition of guanosine 3',5' cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII), with a Pic50 value of 7.2 for cGMP, and can be used in the study of diarrheal diseases.

AP5 sodium is a selective, potent, orally active GPR40 receptor agonist that exhibits positive allosteric modulation of endogenous ligands (AgoPAM). sodium exhibits potential for the study of type II diabetes.

AP-C2 is a potent small molecule guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII) inhibitor with a pIC50 of 5.2 for cGKII.

T-5224 is a transcription factor c-Fos AP-1 inhibitor, which specifically inhibits the DNA binding activity of c-Fos c-Jun without affecting other transcription factors.

AP-C3 is a potent inhibitor of guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII), exhibiting a pIC50 value of 6.3 and demonstrating only weak inhibition of cGKII-dependent anion secretion [1].

AP-C4 is a selective inhibitor targeting guanosine 3′,5′-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII), exhibiting a pIC50 value of 5.2. Conversely, AP-C3 does not inhibit cGKII-mediated anion secretion [1].

AP-C6 is a potent inhibitor of guanosine 3',5'-cyclic monophosphate (cGMP)-dependent protein kinase II (cGKII), exhibiting a pIC50 of 6.5. It inhibits human cGKII activity in vitro in a concentration-dependent manner and potentiates cAMP signaling through phosphodiesterase (PDE) inhibition [1].

NPEC-caged-D-AP5 is a NMDA receptor antagonist.

1,3,5-Trihydroxy-4-prenylxanthone is a relatively potent inhibitor of phosphodiesterase type 5 (PDE5), with an IC50 value of 3.0 μM; it shows in vitro inhibitory activity against acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), with IC50 valu

AP5 is a potent and selective agonist for the GPR40 receptor with positive allosteric modulation of endogenous ligands (AgoPAM). AP5 demonstrates a rat hIP1 EC50 of 0.49 nM against the GPR40 receptor.

12(S)-HpETE is a monohydroperoxy polyunsaturated fatty acid (PUFA) produced by the action of platelet or leukocyte 12-lipoxygenase (12-LO) on arachidonic acid. It activates human blood leukocyte 5-LO, resulting in the synthesis of 5(S)-HETE, leukotriene B4 (LTB4), and 5(S),12(S)-DiHETE. Rat lung metabolizes 12(S)-HpETE to 8,11,12- and 10,11,12-trihydroxyeicostrienoic acids. 12(S)-HpETE is the mediator of many biological functions, including induction of c-fos and c-jun, activation of AP-1, and endothelium-dependent vasoconstriction. It mediates the inhibitory synaptic response to FMRF-amide in Aplysia sensory neurons and inhibits Ca2+/calmodulin-dependent protein kinase II from rat brain cortex.

15(S)-HpETE is a monohydroperoxy polyunsaturated fatty acid (PUFA) produced by the action of 15-lipoxygenase (15-LO) on arachidonic acid. It is either metabolized to 14,15-leukotriene A4 [1] or reduced to 15(S)-HETE by peroxidases.[2] [1] 15(S)-HpETE mediates a number of biological functions including the induction of c-fos and c-jun, and activation of AP-1. [3] 15(S)-HpETE inhibits prostacyclin synthesis in porcine aortic microsomes and bovine endothelial cells, and can cause the suicide inactivation of porcine 12-LO.[2][4][5]

BGC-20-1531 hydrochloride(1186532-61-5 free base) (GTPL3380 hydrochloride) is a EP4 antagonist for the treatment of acute migraine.

L-AP5 is a NMDA antagonist.

DL-AP5 Sodium salt is a NMDA receptor antagonist.

D-AP5 (D-APV) is a NMDA receptor antagonist.

DL-AP5 is the racemic form of a selective N-methyl-D-aspartate (NMDA) receptor antagonist with anticonvulsant effects.

3-O-Methylgallic acid (3,4-Dihydroxy-5-methoxybenzoic acid) reduces cell proliferation in Caco-2 cells(IC50 = 24.1 μM) more effectively than anthocyanins and may offer protection against colon cancer after its formation in the gut. 3-O-Methylgallic acid inhibits transcription factors NF-κB, AP-1, STAT-1, and OCT-1 which are known to be activated in colorectal cancer.

AP-521, a 5-HT1A receptor antagonist, is used potentially for the treatment of anxiety.